A mini review of curcumin and TRPM2 channel: Focus on oxidative neurotoxicity

Abstract

Several neuronal diseases are induced by the induction of apoptosis/cell death and reactive oxygen species (ROS) via the accumulation of excessive free Ca2+ into mitochondria. The Na+ and Ca2+ permeable TRPM2 cation channels are activated by oxidative stress. The TRPM2-mediated Ca2+ influx induces excessive generation of mitochondrial ROS, apoptosis, and inflammation. The actions are modulated by the treatment of antioxidant plants. Curcumin (CURC) is a natural yellow antioxidant. Results of recent studies have indicated that CURC acted protective properties through the inhibition of TRPM2 on the hypoxia, anti-tumor, antioxidant, anti-inflammatory actions in tumor, neuronal, retinal, kidney, and hepatocyte cells. However, the treatment of CURC induced oxidant and TRPM2 stimulator actions in tumor cells. The protective actions of CURC via modulation of oxidative stress and TRPM2 channel on the ROS generation, inflammation, and cell death in neuronal cells and mice retina have been recognized. In conclusion, the present data of TRPM2 demonstrated that the physiologic balance between the neuronal and retinal diseases was arranged in the kidney, neuronal cells and retina by the TRPM2 channels-stimulation mediated Ca2+ influx. However, the treatment of CURC induced protective action through the inhibition of TRPM2 on the inflammatory, oxidant, and apoptotic pathways in the cells. Tumor cells were killed through the stimulation of TRPM2 by CURC. It seems that the TRPM2 stimulator and inhibitor actions of CURC are cell specific.